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Abstract
In the present study, we investigated the cognitive improvement effects and its mechanisms of krill oil (KO) in Aβ25–35-induced Alzheimer’s disease (AD) mouse model. The Aβ25–35-injected AD mouse showed memory and cognitive impairment in the behavior tests. However, the administration of KO improved novel object recognition ability and passive avoidance ability compared with Aβ25–35-injected control mice in behavior tests. In addition, KO-administered mice showed shorter latency to find the hidden platform in a Morris water maze test, indicating that KO improved learning and memory abilities. To evaluate the cognitive improvement mechanisms of KO, we measured the oxidative stress-related biomarkers and apoptosis-related protein expressions in the brain. The administration of KO inhibited oxidative stress-related biomarkers such as reactive oxygen species, malondialdehyde, and nitric oxide compared with AD control mice induced by Aβ25–35. In addition, KO-administered mice showed down-regulation of Bax/Bcl-2 ratio in the brain. Therefore, this study indicated that KO-administered mice improved cognitive function against Aβ25–35 by attenuations of neuronal oxidative stress and neuronal apoptosis. It suggests that KO might be a potential agent for prevention and treatment of AD.
Highlights
Amyloid beta peptide (Aβ) is a major pathological feature in Alzheimer’s disease (AD), and it is widely accepted as a cause of AD [1]
Mice-administered with Krill Oil (KO) and donepezil significantly increased the latency time to enter the brightly chamber, compared with control group. These findings indicated that administration of KO attenuated passive avoidance ability in Aβ25–35 -induced AD mouse model
We evaluated the effect of KO on cognitive impairment in an Aβ25–35 induced- AD
Summary
Amyloid beta peptide (Aβ) is a major pathological feature in Alzheimer’s disease (AD), and it is widely accepted as a cause of AD [1]. Accumulations of Aβ induce neuronal oxidative stress through over-productions of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Neuronal oxidative stress leads to neuroinflammation, mitochondrial dysfunction, and DNA/RNA damages in the brain [2,3]. Neuronal oxidative stress induced by accumulation of Aβ leads to neuronal cell death by stimuli of the apoptotic signaling [4]. Aβ leads to neuronal oxidative stress and neuronal apoptosis, resulting in cognitive impairment and memory deficit. In the treatment of AD, donepezil has been approved by Food and Drug Administration and widely prescribed for AD
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